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【英文】世卫组织报告:全球肿瘤报告(614页)

英文研究报告 2020-06-29 3 管理员

Many gene variants that interact  with environmental agents have  been identified. However, the assessment of causal evidence is often uncertain, because of the very  large sample sizes required to investigate interactions. For each of  the key characteristics of carcinogens, genes with inherited variants  can be found (Table 3.3.1), but the  real impact of these variants in modulating the effect of environmental  exposures is largely unknown. Simonds et al. [8] performed a  systematic review of published literature from two databases of genetic  association studies: the HuGE literature finder and the Cancer GenomeWide Association and Meta Analyses Database (Cancer GAMAdb). Of  3019 articles identified in the searches, only 272 articles met the inclusion  criteria.

In both searches, the majority  of the publications examined gene– environment interactions in cancers  of the colon, rectum, colorectum,  breast, or lung. The interactions examined most frequently included  environmental factors categorized  as energy balance (e.g. indicated by  body mass index, diet), exogenous  hormonal factors (e.g. oral contraceptives), endogenous hormonal factors  (e.g. indicated by menopausal status),  particular chemical exposures (e.g.  consumption of grilled meats), and  lifestyle factors (e.g. smoking, alcohol  consumption) (Fig. 3.3.4). 

Interestingly, the majority of the  interactions examined used loci  from candidate gene studies, and  none of the studies were genomewide interaction studies (i.e. studies  based on genome-wide association  studies [GWAS]). The magnitudes  of the interactions reported were  modest, as is usually the case in  the literature on gene–environment  interactions in cancer: the risks increased or decreased by 20–50%  in carriers of the minor allele compared with wild-type individuals for  the same exposure [9] (some examples are given below).

【英文】世卫组织报告:全球肿瘤报告(614页)

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